Wei Zhang Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Assistant Professor - Tenure Track
faculty
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Biography and Research Information
OverviewAI-generated summary
Wei Zhang's research focuses on molecular and cellular mechanisms underlying vascular diseases and inflammation. His work investigates the role of specific genes and signaling pathways in conditions such as atherosclerosis and vascular senescence. Recent publications include studies on the function of novel long noncoding RNAs in promoting vascular smooth muscle inflammation and the cooperative roles of MKL1 and p38MAPK in vascular senescence and abdominal aortic aneurysm development.
Further research explores the protective mechanisms in cardiomyocytes, specifically how TEAD1 prevents necroptosis through the regulation of nuclear DNA-encoded mitochondrial genes. Zhang also investigates therapeutic strategies, including the use of biomimetic Prussian blue analogues for scavenging reactive oxygen species and mitigating inflammation, and the anti-atherosclerotic effects of glycosides from Buyang Huanwu Decoction via the JAK/STAT signaling pathway.
His work also extends to the development of advanced biosensing technologies, such as an electrochemical biosensor for the sensitive detection of Staphylococcus aureus utilizing SRCA-CRISPR/Cas12a. Collaborations with researchers at the University of Arkansas for Medical Sciences, including Jeanne Y. Wei and Gohar Azhar, contribute to his research network. Zhang's scholarly output is recognized by a high h-index of 46, with over 297 publications and 6,548 citations.
Metrics
- h-index: 46
- Publications: 472
- Citations: 6,681
Selected Publications
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Survival benefit associated with liver transplantation for hepatocellular carcinoma based on tumor burden scores at listing (2025)
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Neutrophil Biomarkers Can Predict Cardiotoxicity of Anthracyclines in Breast Cancer (2024)
Collaboration Network
Top Collaborators
- Prime editing in mice reveals the essentiality of a single base in driving tissue-specific gene expression
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- <i>INKILN</i> is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10
- CRISPR-Cas9 Long-Read Sequencing for Mapping Transgenes in the Mouse Genome
- Prime editing in mice reveals the essentiality of a single base in driving tissue-specific gene expression
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- CRISPR-Cas9 Long-Read Sequencing for Mapping Transgenes in the Mouse Genome
- Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury
- Identification and validation of key long non-coding RNAs in resveratrol protect against IL-1β-treated chondrocytes via integrated bioinformatic analysis
- Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury
- Identification and validation of key long non-coding RNAs in resveratrol protect against IL-1β-treated chondrocytes via integrated bioinformatic analysis
- Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury
- Identification and validation of key long non-coding RNAs in resveratrol protect against IL-1β-treated chondrocytes via integrated bioinformatic analysis
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes
- YAP1/TEAD1 upregulate platelet-derived growth factor receptor beta to promote vascular smooth muscle cell proliferation and neointima formation
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- <i>INKILN</i> is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10
- Prime editing in mice reveals the essentiality of a single base in driving tissue-specific gene expression
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- <i>INKILN</i> is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10
- MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
- <i>INKILN</i> is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10
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